Myocardial infarction during giant cell arteritis: A cohort study.


Journal

European journal of internal medicine
ISSN: 1879-0828
Titre abrégé: Eur J Intern Med
Pays: Netherlands
ID NLM: 9003220

Informations de publication

Date de publication:
07 2021
Historique:
received: 24 11 2020
revised: 02 02 2021
accepted: 04 02 2021
pubmed: 22 2 2021
medline: 24 7 2021
entrez: 21 2 2021
Statut: ppublish

Résumé

Cardiovascular risk is increased in giant cell arteritis (GCA). We aimed to characterize myocardial infarction (MI) in a GCA cohort, and to compare the GCA and non-GCA population affected by MI. In patients with a biopsy-proven diagnosis of GCA between 1 January 2001 and 31 December 2016 in Côte D'Or (France), we identified patients with MI by crossing data from the territorial myocardial infarction registry (Observatoire des Infarctus de Côte d'Or) database. Five controls (non-GCA + MI) were paired with one case (GCA + MI) after matching for age, sex, cardiovascular risk factors and prior cardiovascular disease. MI were characterized as type 1 MI (T1MI), resulting from thrombus formation due to atherothrombotic disease, or type 2 MI (T2MI), due to a myocardial supply/demand mismatch. GCA-related MI was defined as MI occurring within 3 months of a GCA flare (before or after). Among 251 biopsy-proven GCA patients, 13 MI cases were identified and paired with 65 controls. MI was GCA-related in 6/13 cases, accounting for 2.4% (6/251) of our cohort. T2MI was more frequently GCA-related than GCA-unrelated (80% vs. 16.7%, p = 0.080), and GCA diagnosis was the only identified triggering factor in 75% of GCA-related T2MI. GCA-unrelated MI were more frequently T1MI and occurred in patients who had received a higher cumulative dose of prednisone (p = 0.032). GCA was not associated with poorer one-year survival. GCA-related MI are mainly T2MI probably caused by systemic inflammation rather than coronaritis. GCA-unrelated MI are predominantly T1MI associated with atherothrombotic coronary artery disease.

Sections du résumé

BACKGROUND
Cardiovascular risk is increased in giant cell arteritis (GCA). We aimed to characterize myocardial infarction (MI) in a GCA cohort, and to compare the GCA and non-GCA population affected by MI.
METHODS
In patients with a biopsy-proven diagnosis of GCA between 1 January 2001 and 31 December 2016 in Côte D'Or (France), we identified patients with MI by crossing data from the territorial myocardial infarction registry (Observatoire des Infarctus de Côte d'Or) database. Five controls (non-GCA + MI) were paired with one case (GCA + MI) after matching for age, sex, cardiovascular risk factors and prior cardiovascular disease. MI were characterized as type 1 MI (T1MI), resulting from thrombus formation due to atherothrombotic disease, or type 2 MI (T2MI), due to a myocardial supply/demand mismatch. GCA-related MI was defined as MI occurring within 3 months of a GCA flare (before or after).
RESULTS
Among 251 biopsy-proven GCA patients, 13 MI cases were identified and paired with 65 controls. MI was GCA-related in 6/13 cases, accounting for 2.4% (6/251) of our cohort. T2MI was more frequently GCA-related than GCA-unrelated (80% vs. 16.7%, p = 0.080), and GCA diagnosis was the only identified triggering factor in 75% of GCA-related T2MI. GCA-unrelated MI were more frequently T1MI and occurred in patients who had received a higher cumulative dose of prednisone (p = 0.032). GCA was not associated with poorer one-year survival.
CONCLUSIONS
GCA-related MI are mainly T2MI probably caused by systemic inflammation rather than coronaritis. GCA-unrelated MI are predominantly T1MI associated with atherothrombotic coronary artery disease.

Identifiants

pubmed: 33610415
pii: S0953-6205(21)00038-8
doi: 10.1016/j.ejim.2021.02.001
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

30-38

Informations de copyright

Copyright © 2021. Published by Elsevier B.V.

Auteurs

Hélène Greigert (H)

Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Department of Vascular Medicine, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000 Dijon, France.

Marianne Zeller (M)

PEC2, EA 7460 Dijon, France.

Alain Putot (A)

PEC2, EA 7460 Dijon, France; Department of Geriatric Internal Medicine, Dijon University Hospital, Dijon, France.

Eric Steinmetz (E)

Department of Cardiovascular and Thoracic Surgery, Dijon University Hospital, Dijon, France.

Béatrice Terriat (B)

Department of Vascular Medicine, Dijon University Hospital, Dijon, France.

Maud Maza (M)

PEC2, EA 7460 Dijon, France.

Nicolas Falvo (N)

Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France.

Géraldine Muller (G)

Department of Internal Medicine and Systemic Diseases, Dijon University Hospital, Dijon, France.

Louis Arnould (L)

Department of Ophthalmology, Dijon University Hospital, Dijon, France.

Catherine Creuzot-Garcher (C)

Department of Ophthalmology, Dijon University Hospital, Dijon, France.

André Ramon (A)

Department of Rheumatology, Dijon University Hospital, Dijon, France.

Laurent Martin (L)

Department of Pathology, Dijon University Hospital, Dijon, France.

Georges Tarris (G)

Department of Pathology, Dijon University Hospital, Dijon, France.

Tibor Ponnelle (T)

Cypath pathology center, Dijon, France.

Sylvain Audia (S)

Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000 Dijon, France.

Bernard Bonnotte (B)

Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000 Dijon, France.

Yves Cottin (Y)

Cardiology Department, Dijon University Hospital, Dijon, France.

Maxime Samson (M)

Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000 Dijon, France. Electronic address: maxime.samson@u-bourgogne.fr.

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